Liu J H, Wei S, Blanchard D K, Djeu J Y
H. Lee Moffitt Cancer Center, University of South Florida College of Medicine, Department of Medical Microbiology, Tampa 33612.
Cell Immunol. 1994 Jun;156(1):24-35. doi: 10.1006/cimm.1994.1150.
NK cells can recognize and lyse target cells without restriction by the MHC. The molecular interaction responsible for NK cell recognition is poorly understood. It has been frequently suggested that the loss of beta 2 integrin in immune competent cells may lead to dysfunction due to inadequate cell-cell interaction. We examined the role of lymphocyte functional adhesion molecule-1 in the function of a human natural killer leukemia cell line, YT-1. A mutant YT-1(-) cell subclone showed an absence of killing activity against a B lymphoma cell line, compared with that against a CD11a/CD18 positive parental cell line, YT-1(+) cells. We found that this loss of cytotoxicity was correlated with lack of surface expression of CD11a/CD18 molecules due to the mutation of the CD18 gene. Using gene transfer experiments, we provide strong evidence demonstrating that CD18 transfection to this mutant NK cell line, YT-1(-), restored the surface expression of CD11a/CD18, and this restoration was accompanied by reexpression of cytotoxic function.
自然杀伤细胞（NK细胞）能够识别并裂解靶细胞，不受主要组织相容性复合体（MHC）的限制。目前对负责NK细胞识别的分子相互作用了解甚少。人们经常认为，免疫活性细胞中β2整合素的缺失可能由于细胞间相互作用不足而导致功能障碍。我们研究了淋巴细胞功能粘附分子-1在人自然杀伤白血病细胞系YT-1功能中的作用。与针对CD11a/CD18阳性亲代细胞系YT-1(+)细胞相比，突变的YT-1(-)细胞亚克隆对B淋巴瘤细胞系缺乏杀伤活性。我们发现，这种细胞毒性的丧失与由于CD18基因突变导致的CD11a/CD18分子表面表达缺失有关。通过基因转移实验，我们提供了有力证据表明，将CD18转染到这种突变的NK细胞系YT-1(-)中，可恢复CD11a/CD18的表面表达，并且这种恢复伴随着细胞毒性功能的重新表达。
